Abstract
Aim: To study effects of recombinant human growth hormone (rhGH) on growth hormone-insulin-like growth factor axis (GH-IGFs) of human gastric cancer cell in vivo in order to reveal part mechanism of growth effects of rhGH on gastric cancer. Methods: Nude mice were randomly divided into control group, cisplatin (DDP) group, rhGH group and DDP + rhGH group after human gastric cancer xenograft model of node mice was successfully founded and drugs were used for 6 days. We investigated volume of tumor, inhibitory rate of tumor and cell cycle by slide gauge and flow cytometry. In addition, We also respectively investigated insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) of blood serum of nude mice, IGF-ImRNA, insulin-like growth factor-I receptor (IGF-IR) mRNA and IGFBP-3 mRNA of xenograft of nude mice by enzyme linked immunosorbent assay (ELISA) and semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) on the first day of completing use of drugs later. Results: Tumor grew obviously slowly and tumor inhibitory rate obviously rose in DDP group and DDP + rhGH group compared with control group and rhGH group (p p p < 0.05). Expressions of IGF-I mRNA and IGF-IR mRNA were not obviously different in all groups. But expression of IGFBP-3 mRNA obviously increased in rhGH group, DDP group and DDP + rhGH group compared with control group; meanwhile, expression of IGFBP-3 mRNA also obviously increased in DDP + rhGH group compared with control group, DDP group and rhGH group. Conclusion: Our results indicated rhGH in short-time use did not improve proliferation of human gastric cancer cells and its mechanism was possible that rhGH in short-time use raised simultaneously IGF-I and IGFBP-3 of blood serum and increased IGFBP-3 mRNA, but degraded ratio of IGF-I and IGFBP-3 of blood serum in human gastric cancer cells.
Highlights
The effect of growth hormone/insulin-like growth factor (GH/IGF) axis on normal cells was very clear; many evidences manifested that GH/IGF axis promoted growth of tumor tissue [1] [2]
Volume of Tumor and Tumor Inhibitory Rate Tumor grew obviously slowly and tumor inhibitory rate obviously rose in DDP group and DDP + recombinant human growth hormone (rhGH) group compared with control group and rhGH group (p < 0.05); but they were not remarkably different between DDP group and DDP + rhGH group or between control group and rhGH group (Table 2)
enzyme linked immunosorbent assay (ELISA) Detection As shown in Table 3, insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) of blood serum of nude mice obviously stepped up in rhGH group or DDP + rhGH group compared with Control group or DDP group but ratio of IGF-I and insulin-like growth factor binding protein (IGFBP)-3 obviously lowered and there was significant difference among them
Summary
The effect of growth hormone/insulin-like growth factor (GH/IGF) axis on normal cells was very clear; many evidences manifested that GH/IGF axis promoted growth of tumor tissue [1] [2]. Lots of overseas clinical data showed that hGH did not improve cancer growth and could decrease peroperative complications incidence and death rate in postoperative patients with gastrointestinal malignant tumor [9]-[13]. 1% of IGF was free and effective in vivo, while 99% was combined with insulin-like growth factor binding protein (IGFBP). We analyzed contents of insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3) of blood serum and expression IGF-ImRNA, insulin-like growth factor-I receptor (IGF-IR) mRNA, and IGFBP-3 mRNA of transplantation tumor of nude mice with gastric cancer after rhGH was used in nude mice for short term. Our experiment results would reveal part mechanism of growth effects of rhGH on gastric cancer
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.